Download - 2012 Annual Glycemic Control (Adult)
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Glycemic Control
Annual Competency Review
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What is Diabetes
Metabolic diseases characterized by inappropriate hyperglycemia
resulting from defects in insulin secretion, insulin action, or both.
(ADA, 2003)
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Overview of Food Metabolism
Every cell in the human body
requires energy to function (24
hours/day)
The bodys primary source of
energy is glucose (blood sugar)
Glucose enters the cells with the
help ofinsulin
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FOOD SUGAR
Carbohydrates are the bodys
primary source of energy
Glucose is the end product ofcarbohydrate metabolism
Protein and fats only have a
minimal effect on blood glucose
levels.
LIVER SUGAR
In a fasting state, the liver
produces glucose from 3 sources of
stored energy
Glucogenoloysis
Glycogen (a form of glucose
stored in the liver andmuscles)
Gluconeogenesis
Amino acids (supplied from
muscle tissues)
Glycerol (supplied from fat)
Sources of Glucose
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What is InsulinInsulin is a hormone produced by the beta cells in
the pancreas.
In response to increased glucose levels, the
pancreas releases insulin into the blood stream to
help glucose enter the cells, subsequently lowering
blood glucose levels
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How Does Insulin Work
Insulin acts like a key that stimulates the cells of thebody to take up glucose (blood sugar), so that theyhave the energy to do their work.
When insulin reaches the insulin receptor sites theglucose is able to enter into the cell.
CELL WALL
Insulin Receptor Site
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The liver and the pancreas work together to control the bodys
fuel supply. After a meal, an individuals blood glucose levelrises. the pancreas releases insulin into the bloodstream tohelp the glucose enter the cells and to signal the liver to stopproducing extra glucose, subsequently lowering the bloodglucose levels. When the blood glucose level is lowered, insulinreleased from the pancreas is reduced.
NORMAL
BLOOD
SUGAR
INSULIN LIVER SUGAR
Maintaining Glucose Balance
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Classification of Diabetes
Type 1
Diabetes Type 1 is characterized by the destruction of beta
cells. Without beta cells, the body is unable to produceinsulin. Type 1 patients can get into trouble quickly when
you withhold their insulin. Even when NPO, the liver
continues to supply glucose for the cells and insulin is
required to allow the cells to utilize the insulin
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Diabetes Type 2 is characterized by insulin resistance. The
pancreas actually makes insulin, but the cells do norecognize or respond to the insulin very well, increasing
the patients insulin requirements. Eventually, the beta
cells become overworked and begin to dysfunction. At
that point the pancreas is unable to produce enough
insulin to keep blood glucose levels normal.
Type 2
Classification of Diabetes
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Classification of Diabetes
Gestational Diabetes Diabetes during pregnancy
Consists of women who develop gestational diabetes
(carbohydrate intolerance of variable severity with
the onset or first recognition during pregnancy Pregnancy is an insulin-resistant or
diabetogenic state, normally. However, there is
evidence that women who develop GDM
secrete less insulin in response to a glucose
load than women who do not develop GDM
Diabetes in the Life Cycle and Research, AADE, 2003
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SIGNS AND SYMPTOMS OF
HYPERGLYCEMIA
Polyuria (excessive urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger) Blurred vision
Weight loss
Fatigue Muscle cramps
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Diabetic Ketoacidosis (DKA) is caused by a profound insulin deficiency. Although small amounts of insulin may be
circulating, the presence of large amounts of stress hormones (glucagon, catecholamines, cortisol, and growth hormone)
renders the insulin less effective. Carbohydrate, protein, and fat metabolism are all markedly affected. Prolonged insulin
deficiency and hormonal influences lead to the breakdown of fat in the body. Normally, ketoacids can be used by neural
and muscle tissue for energy metabolism. However the amount of ketoacids is too great. As a result, the normal
pathway becomes saturated and the pH of the blood falls.
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Signs and Symtoms of DKA
General weakness Signs of dehydration
Hypoghermia (unless an infections is present)
Acetone / fruity breath
Abdominal tenderness
Diminished breath sounds
Decreased reflexes
Blood glucose usually > 300 mg/dL
Arterial pH < 7.3
Urine and serum ketone positive
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Hyperosmolar Hyperglycemic Nonketotic Syndrome (HHNS) is characterized by high plasma osmolarity (SEVERE
dehydration volume depletion) and blood glucose in excess of 600. The presence of endogenous insulin in type 2
diabetes suppresses the lipolysis that leads to the production of ketone bodies and subsequent ketoacidosisassociated with type 1 diabetes.
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Signs and Symptoms of HHS
Symptoms of severe dehydration (orthostatic
hypotension, rapid breathing, rapid heart rate,
low B/P, and poor skin turgor)
Decreased level of consciousness
Stroke-like symptoms
Blood glucose usually > 600 mg/dL
Absence of ketosis
Arterial pH > 7.30 (no acidosis)
M b li S R
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Metabolic Stress Response
The stressresponse is the name given to the hormonal and metabolicchanges which follow injury, trauma
or illness. This is part of the systemicreaction to illness or injury which leads to hyperglycemia and
encompasses a wide range of endocrinological,immunological and hematological effects. This means you
dont have to have diabetes to be at risk for high blood sugars.
Hyperglycemia is associated with a wide range of physiologic derangements. This diagram illustrates how the
adverse effects of hyperglycemia may contribute to suboptimal patient outcomes, including high rates of
infection in hospitalized patients, disability, poor wound healing, increased mortality in some patientpopulations, and adverse health economic outcomes such as longer lengths-of-stay and increased costs.
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New Glycemic Targets
ICU: Start insulin infusion if BG>180
Goal: 140-180 mg/dL
Non- ICU:
Pre-meal:
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Optimizing Insulin Use
In order to optimize the use of insulin we should look at how the body uses
insulin and mimic the pattern of normal pancreatic secretions as close as possible.
So, lets look at how the pancreas works.
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Nutritional (Bolus) Insulin
Later, when we eat again, another burst ofinsulin is secreted from the pancreas intothe blood. The liver stops releasing storedsugar and begins to build up its stores for
later use. Nutritional intake includes: oral feeding, IVdextrose, parenteral nutrition (TPN), tubefeedings, and nutritional supplements (Ensure)
We mimic this action with rapid- or fast-acting
insulins ordered with meals
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Corrections Insulin CORRECTION INSULIN
We also use rapid- and fast-acting
insulins to correct high blood sugars
and bring them down elevated to a
normal level
Old term sliding scale
Do not holdeven if the patient
does not eat because the dose should only be enough to
reduce elevated sugars to within normal limits
If a correction dose of insulin of insulin causes hypoglycemia,notify the physician. The correction scale may be too
aggressive
Dose can be ordered as decrease bedtime dose by half or
even as Hold bedtime dose to prevent late-night
hypoglycemia events
FSBS < 60 give 1 amp of D50151-200 give 2 unit
201-250 give 4 units
251-300 give 6 units
301-350 give 8 units
>350 give 10 units, call the Dr. andrepeat FSBS in one hour
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Whats wrong with sliding scale?
The traditional sliding scale regimens do not contain basal or nutritional doses of insulin. They only consist
of pre-meal and bedtime monitoring of the patients blood glucose levels and giving a dose of insulin if the
glucose level is too high. This out-dated concept was once a standard, but a sliding scale scheme, by itself,
cannot keep blood sugars consistently in the target range.
With Sliding Scale Regimens, glycemic control is rarelyassessed. Notice that the fingersticks are taken at the
lowest levels of the day (just before meals) then the patient eats and the blood sugar immediately begins to
rise. Not only are the hyperglycemic events completely undetected, but the patient stays at elevated levels for
most of the day; putting him/her at risk for complications such as infections and poor wound healing.
Sliding Scale Regimens are usually not individualized to meet a patients specific insulin resistance level. They
tend to be one-size-fits-all regimens that do not take into account individual variability. This method is reactive
instead ofproactive (treats hyperglycemia but doesnt prevent it) and is NOT recommended for use as
monotherapy for greater than 48 hours. Clinical evidence indicates that Sliding Scale Insulin as a primary
therapy is ineffective and potentially dangerous and frequently causes a harmful rollercoaster effect.
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Nutritional and Correction insulin doses, should be ordered using the
SAME type of insulin and should be given together, in the same syringe, atthe same time to prevent unnecessary sticks (usually given just prior toeating)
Nutritional insulin is the only insulin that is dependent upon whether the
patient eats or not Basal insulin should always be given according to the order (even if NPO or
if FSBS is low)
Correction insulin should always be given (even if NPO)
A physicians order required for holding insulin
Basal/Bolus Concepts
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NEUROGENIC SYMPTOMS NEUROGLYCOPENIC SYMPTOMS
Adrenergic
Heart pounding
Nervousness and anxiety
Shakiness and tremulousness
Cholinergic
Hunger
Sweating
Tingling
Behavioral changes
Brain damage
Confusion
Death
Difficulty thinking / slurred speech
Emotional liability
Fatigue
Loss of consciousness Seizures
Weakness / uncoordination
Occurs in early or mild hypoglycemia
Patient is ABLE to self-treat
Response to the increase in epinephrine
Occurs in late or severe hypoglycemia
Patient is UNABLE to self-treat
Response to the decrease in glucose to the brain
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Causes of Hypoglycemia
Too much medication Insulin given at an inappropriate time
Lack of coordination between
transportation and nursing.
Delaying of food lack of coordination between dietary and nursing leads
to mistiming of insulin dosage with respect to food
Instruct patient to inform staff when ordering or
receiving food. Not eating after taking diabetes medication
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Causes of Hypoglycemia
Everyone knows that too much insulin can lead to hypoglycemia butwe need to also remember that over treating hypoglycemia can be
just as dangerous, causing rebound hyperglycemia and the bloodsugar rollercoaster effect.
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Caution should betaken with multiple,consecutive dosing
of Regular insulin
Onset: - 1 hourPeak: 1-2 hours
Duration : 5-8 hour
Causes of Hypoglycemia
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Delayed response and late snowballing from repeated insulin doses mayoccur among patients with poor perfusion of subcutaneous sites. Insulinbuilds up in the tissues and is absorbed simultaneously once perfusion isrestored leading to overdosing of insulin and hypoglycemia..
Hypoalbuminemia
Edema
Hypotension
Pressors
Renal failure or renal insufficiency also has a serious impact on circulatinginsulin levels by reducing insulin clearance and allowing insulin toaccumulate in the circulation
Causes of Hypoglycemia
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Causes of Hypoglycemia
Be Aware of Hypoglycemic Unawareness
The early signs of hypoglycemia occur due to a response to the increase in epinephrine (adrenaline)
and can be used as a warning signal for prompt treatment. However, over the course of diabetes, or
following repeated episodes of hypoglycemia, patients can develop a delayed or diminished response
to epinephrine resulting in reduced hypoglycemic symptom awareness. This decreases response time
before severe symptoms appear and places patient at risk for unrecognized hypoglycemia 24 to 48
hours after an episode of hypoglycemia.
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False Lows
Sometimes a person may have symptoms of lowblood sugar levels, but the blood sugar levels are
not actually low. This is called a false reaction.The hormone adrenaline is not just releasedwhen blood sugar drops too lowits alsoreleased when blood sugar levels fall tooquickly.
There is no need to treat a false reaction. Justhave the patient lie down for about 10 minutesand the symptoms will subside and continue tomonitor the patients blood sugar and symptomsuntil they are stabilized.
Causes of Hypoglycemia
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Treating Hypoglycemia
Use the 15/15 Rule or Fast 15 Give 15g. of fast-acting carb and wait 15 minutes before retaking FSBS--
-repeat if needed---if a meal is not available within 30 to 60 minutes,give the patient a snack with protein (P/B and crackers, cheese andcrackers, meat sandwich, glass of milk,etc) to prevent hypoglycemiafrom reoccurring
15 grams carbs or ONE carbohydrate choice 3 glucose tablets
4 oz of non-diet cola
4 oz of fruit juice DO NOT ADD SUGAR
an amp of D50 (always follow physicians order)
Limit treatment to 15 grams at a time.
Over-treating hypoglycemia causes the
roller coaster affect.
15 grams of carbs elevates the blood sugar 30-40 points and is usuallysufficient for most events
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Able to Eat
Adult Hypoglycemia orders
Provide aFAST 15
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Unable to Eat
IV Present
Adult Hypoglycemia orders
Its Time
for D50
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Unable to Eat
No IV Present
Adult Hypoglycemia orders
IM
Glucagon
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HypoglycemiaFinish What You Started
V/S + Neuro Check 15 minutesafter each treatment or until stable
Notify MD
Document: interventions, patient response,and MD notification
If FSBS < 40 and the patient is asymptomatic, redo thetest at another site (venous specimen preferred)
Identify Patient as High Risk for Hypoglycemia for next
24 hours
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Close Monitoring
FSBSs must be retaken if the correction insulinis not administered within one hour of FSBS
FSBSs should be repeated if the glucometer
reads "HI" (>600) or "LO" (
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Patient Education: Walk & Talk
Diabetes Dia-log
Heres your basal insulin
Mrs. Jones. Its a long-acting insulin that covers
your fasting insulinrequirements.
I need you to practicedrawing it up and giving it
to yourself.
Ill be right here if you
need me.
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The Power of One
Become A Glycemic Control Advocate
Promote best practicesClarify any orders that you feel areinaccurate or inappropriate
Initiate treatment changes to coincide withstatus changes or treatment failureCommunicate to the members of yourhealthcare teamListen to the patient---they usually know
more about controlling their own glucose thanwe do. Do not ignore their comments.Instead, utilize them to improve the patients
care